ArticleNeuron2021
Akt-mTOR hypoactivity in bipolar disorder gives rise to cognitive impairments associated with altered neuronal structure and function.
Article in Neuron, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Efficacy of spironolactone as adjunctive therapy to sodium valproate in bipolar-I disorder: A double-blind, randomized, placebo-controlled clinical trial.Brain and behavior · 2023Trial
- Roles of autophagy in brain homeostasis and disease.Nature neuroscience · 2026Review
- Integrated Expression and Bioinformatic Analysis of AKT-Associated lncRNAs Suggests UCA1 as a Candidate Biomarker for Bipolar Disorder.Journal of molecular neuroscience : MN · 2026Article
- Schizophrenia and bipolar disorder risk gene AKAP11 sustains cognitive function by regulating TFEB-mediated autophagy.Cell death and differentiation · 2026Article
- Phosphatase and tensin homolog: A potential target for therapeutic intervention in optic nerve regeneration.Neural regeneration research · 2026Article
- Elevated maternal testosterone induces sex-specific neurodevelopmental changes and ASD-related behavioral phenotypes in rat offspring.Pediatric research · 2026Article
- Sex Differences in Brain Cell Type-Specific Chromatin Accessibility in Schizophrenia.Biological psychiatry · 2026Article
- Disruption of the l-DOPA Receptor Gpr143/OA1-Gene in Mice Creates a Unique Mixed Psychosis-Like Phenotype.Neuropsychopharmacology reports · 2026Article
- Castl: robust identification of spatially variable genes in spatial transcriptomics via an ensemble-based framework.Briefings in bioinformatics · 2026Article
- From energy metabolism to mood regulation: The rise of lactate as a therapeutic target.Journal of advanced research · 2026Review
- Premature aging in serious mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- From synapse to system: mechanistic pathways of neural signaling dysfunction in psychiatric disorders.Frontiers in cell and developmental biology · 2026Review
- Prefrontal spine loss in neuropsychiatric disorders: circuit consequences for cognition.Frontiers in psychiatry · 2026Review
- Differential microRNA profiling of blood L1CAM and bulk extracellular vesicles in bipolar disorder.Epigenomics · 2025Article
- Proposed Mechanistic Axis of Infections and mTOR Hyperactivation: A Multidisciplinary Review of Immune, Rheumatologic, and Psychiatric Links.Children (Basel, Switzerland) · 2025Review
- The 4E-BPs as Translational Regulators in Neurological Disorders: Molecular Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Metabolic plasticity: an evolutionary perspective on metabolic and circadian dysregulation in bipolar disorder.Molecular psychiatry · 2025Review
- Alterations of plasma neural-derived extracellular vesicles microRNAs in patients with bipolar disorder.Psychological medicine · 2025Article
- Inositol Phosphates and Synthesizing Enzymes: Implications in Neurodegenerative Disorders.Biomolecules · 2025Review
- Identification ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
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6 authors.
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Abstract
The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function.
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